casbazaar.blogg.se - Lithium toxicity antidote

Clinical features: polyuria, nocturia, and polydipsia → ↑ risk of dehydrationand subsequent lithium toxicity.Pathophysiology: lithium interferes with ADH signaling → ↓ aquaporins (water channels) on the collecting duct cell's surface → ↓ water molecules are reabsorbed and kidneys are unable to concentrate urine → ↑ free water excretion.Goiter (particularly in second and third trimester of pregnancy ).Caused by the elevation of the calcium-sensing setpoint of the parathyroid glands and induction of parathyroid hormone production.

There is usually no need to discontinue lithium therapy.Lithium-induced hypothyroidism, should be treated with replacement therapy ( levothyroxine).

Thyroid function tests should be performed every 6–12 months during ongoing treatment.

Sinus node dysfunction (most commonly sinus bradycardia).

ECG changes: T-wave depressions (most common), U waves, repolarization abnormalities.

Often decreases spontaneously over time.

Typically occurs when lithium therapy is started or the dose is increased but can occur at any time during the course of treatment.

Nonprogessive, s ymmetric, fine postural tremor in the distal ends of upper extremities.

Adverse effects occur at therapeutic levels ( 0.4–1.0 mEq/L) but tend to be more severe at peak serum concentration of the drug.